@article{90acd4acf3964171b3909e609b404f07,
title = "Network Dynamics Mediate Circadian Clock Plasticity",
abstract = "A circadian clock governs most aspects of mammalian behavior. Although its properties are in part genetically determined, altered light-dark environment can change circadian period length through a mechanism requiring de novo DNA methylation. We show here that this mechanism is mediated not via cell-autonomous clock properties, but rather through altered networking within the suprachiasmatic nuclei (SCN), the circadian “master clock,” which is DNA methylated in region-specific manner. DNA methylation is necessary to temporally reorganize circadian phasing among SCN neurons, which in turn changes the period length of the network as a whole. Interruption of neural communication by inhibiting neuronal firing or by physical cutting suppresses both SCN reorganization and period changes. Mathematical modeling suggests, and experiments confirm, that this SCN reorganization depends upon GABAergic signaling. Our results therefore show that basic circadian clock properties are governed by dynamic interactions among SCN neurons, with neuroadaptations in network function driven by the environment.",
keywords = "automation, autopatcher, in vivo, patch clamp, subcortical, thalamus, whole-cell",
author = "Abdelhalim Azzi and Evans, {Jennifer A.} and Tanya Leise and Jihwan Myung and Toru Takumi and Davidson, {Alec J.} and Brown, {Steven A.}",
note = "Funding Information: A.A. has been supported by the Velux Foundation and the Forschungskredit of the University of Z{\"u}rich. This work has received further support via S.A.B. from the Swiss National Science Foundation, the Velux Foundation, and the Clinical Research Priority Program “Sleep and Health” of the University of Z{\"u}rich. A.A. and S.A.B. are members of the Zurich Neurozentrum, a division of the Life Sciences Z{\"u}rich graduate program. J.A.E. was supported by R01NS091234. A.D. was supported by NIH grants U54NS060659 and S21MD000101, the Georgia Research Alliance, and the NSF Center for Behavioral Neuroscience. T.L. gratefully acknowledges support through the Amherst College Faculty Research Award Program funded by The H. Axel Schupf {\textquoteleft}57 Fund for Intellectual Life. J.M. was supported by RIKEN Incentive Research Project (G1E-54500). T.T. was supported by Ministry of Education, Culture, Sports, Science and Technology in Japan Grants-in-Aid for Scientific Research (25240277, 23111005, 26670165), Strategic International Cooperative Program from the Japan Science and Technology Agency, Intramural Research Grant for Neurological and Psychiatric Disorders of NCNP, and the Takeda Science Foundation. The authors would like to thank Oscar Cervantes-Castanon and Stanford Photonics for assistance. Publisher Copyright: {\textcopyright} 2017 Elsevier Inc.",
year = "2017",
month = jan,
day = "18",
doi = "10.1016/j.neuron.2016.12.022",
language = "English",
volume = "93",
pages = "441--450",
journal = "Neuron",
issn = "0896-6273",
publisher = "Cell Press",
number = "2",
}